A research group led by Dr. Jin-Tu Lou from China has reported that Helicobacter pylori could inhibit intercellular communication of cultured gastric cells. This finding provides a new direction to illuminate the molecular mechanism of the worldwide infectious bacterium in gastric carcinogenesis.
Gap junctions are fundamental structures necessary for cell differentiation, tissular physiology and normal functions of the organs of the body. The loss of functional gap junctions has been described in cancer cells and led to the hypothesis that such type of intercellular communication is involved in the carcinogenesis process. Up to now, a lot of data has been accumulated, confirming that gap junctional intercellular communication (GJIC) is frequently decreased or absent in cancers such as liver cancer, skin cancer, bladder cancer, breast cancer, lung cancer, and so on. However, the change of GJIC in H pylori-associated gastric cancer has been little exploited.
In this article, the researchers treated a human gastric cell line in vitro with intact bacteria and sonicated extracts of two H pylori strains with the virulence protein CagA. These were positive (CagA+) and negative (CagA-), respectively. After overnight treatment, the GJIC of the cells was measured by a technique named fluorescence redistribution after photobleaching (FRAP). The authors found that both CagA+ and CagA- H pylori strains could inhibit the GJIC of gastric cells when compared with a blank group. In addition, the inhibitory effect on the GJIC of gastric cells of CagA+ H pylori was more significant than that of CagA-.
The results of this article provide an innovative direction to develop new drugs for curing gastric cancer. That means drugs able to restore GJIC in cells with deficient gap junction may be used in the prevention and/or treatment of human gastric cancer.